A recent prospective study of post transfusion hepatitis conducted by us has documented not only an inordinate frequency of hepatitis (43%) but a high frequency of chronic sequellae of acute hepatitis (40%) following blood transfusions. The objectives of this program are to prospectively follow a group of previously well characterized patients with post transfusion hepatitis to assess the hazards, if any, of simultaneous transfusion of Hepatitis B Antigen (HBAg) and its antibody (HBAb) and to establish the frequency and natural course of the chronic sequellae of acute hepatitis. It will be an objective of these studies to determine if chronic liver disease is more commonly associated with HBAg positive or negative blood transfusions and to further determine if any specific HBAg subtypes more commonly result in chronic liver disease. Pilot tubes from all units of blood transfused at the UCLA Center for the Health Sciences have been coded and frozen for the past 2 years. Two weeks after transfusion, pilot tubes initially negative for HBAg by counterelectrophoresis were rescreened by radioimmunoassay and red cell agglutination. The recipients of HBAg positive blood units were identified and were followed at 2 week intervals with SGPT, HBAg and HBAb levels for 9 months. Each recipient of HBAg positive blood was matched with a recipient of the same race, age and sex who had received the same number of negative blood units. It is proposed that the 9 month follow up period for the 120 patients in this study be extended for a minimum of 3 years. It is proposed that at montly intervals each of the patients previously know to have developed acute hepatitis be reevaluated clinically as well as biochemically with serial SGPT, HBAg and HBAb levels. Those patients having SGPT elevations in excess of 2 1/2 times the upper limit of our laboratory normal will undergo liver biopsy after 16 weeks of SGPT elevation and if SGPT remains elevated or HBAg levels remain positive, liver biopsies will thereafter be repeated at 12 month intervals. Attempts will be made to correlate the presence or absence of HBAg and specific HBAg subtypes, or the simultaneous transfusion of HBAg and its antibody with the later development of chronic liver disease.